What is Anosognosia?


Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical or psychological (e.g. PTSD, Stockholm syndrome, schizophrenia, bipolar disorder, dementia) condition.

Anosognosia can result from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, it was first named by the neurologist Joseph Babinski in 1914. Phenomenologically, anosognosia has similarities to denial, which is a psychological defence mechanism; attempts have been made at a unified explanation. Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of body parts such as their limbs. The term is from Ancient Greek ἀ- a-, ‘without’, νόσος nosos, ‘disease’ and γνῶσις gnōsis, ‘knowledge’. It is also considered a disorder that makes the treatment of the patient more difficult, since it may affect negatively the therapeutic relationship.


Relatively little has been discovered about the cause of the condition since its initial identification. Recent empirical studies tend to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems.

Anosognosia is relatively common following different causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the manoeuvre of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association with spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and that neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.

Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetics errors and shows “anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him”. This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.


Although largely used to describe unawareness of impairment after brain injury or stroke, the term “anosognosia” is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognise that they have a mental illness. There is evidence that anosognosia related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.


Clinically, anosognosia is often assessed by giving patients an anosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither of the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon; nor are the responses obtained via offline questionnaire capable of revealing the discrepancy of awareness observed from their online task performance. The discrepancy is noticed when patients showed no awareness of their deficits from the offline responses to the questionnaire but demonstrated reluctance or verbal circumlocution when asked to perform an online task. For example, patients with anosognosia for hemiplegia may find excuses not to perform a bimanual task even though they do not admit it is because of their paralysed arms.

A similar situation can happen to patients with anosognosia for cognitive deficits after traumatic brain injury when monitoring their errors during the tasks regarding their memory and attention (online emergent awareness) and when predicting their performance right before the same tasks (online anticipatory awareness). It can also occur among patients with dementia and anosognosia for memory deficit when prompted with dementia-related words, showing possible pre-attentive processing and implicit knowledge of their memory problems. Patients with anosognosia may also overestimate their performance when asked in first-person formed questions but not from a third-person perspective when the questions referring to others.

When assessing the causes of anosognosia within stroke patients, CT scans have been used to assess where the greatest amount of damage is found within the various areas of the brain. Stroke patients with mild and severe levels of anosognosia (determined by response to an anosognosia questionnaire) have been linked to lesions within the temporoparietal and thalamic regions, when compared to those who experience moderate anosognosia, or none at all. In contrast, after a stroke, people with moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.


In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train patients to adjust for their inoperable limbs (though it is believed that these patients still are not “aware” of their disability). Another commonly used method is the use of feedback – comparing clients’ self-predicted performance with their actual performance on a task in an attempt to improve insight.

Neurorehabilitation is difficult because, as anosognosia impairs the patient’s desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.

In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalisation. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.

One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognise their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.

Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.

This page is based on the copyrighted Wikipedia article <https://en.wikipedia.org/wiki/Anosognosia >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is Thought Suppression?


Thought suppression is a psychological defence mechanism. It is a type of motivated forgetting in which an individual consciously attempts to stop thinking about a particular thought.

It is often associated with obsessive-compulsive disorder (OCD). OCD is when a person will repeatedly (usually unsuccessfully) attempt to prevent or “neutralise” intrusive distressing thoughts centred on one or more obsessions. It is also thought to be a cause of memory inhibition, as shown by research using the think/no think paradigm. Thought suppression is relevant to both mental and behavioural levels, possibly leading to ironic effects that are contrary to intention. Ironic process theory is one cognitive model that can explain the paradoxical effect.

When an individual tries to suppress thoughts under a high cognitive load, the frequency of those thoughts increases and becomes more accessible than before. Evidence shows that people can prevent their thoughts from being translated into behaviour when self-monitoring is high; this does not apply to automatic behaviours though, and may result in latent, unconscious actions. This phenomenon is made paradoxically worse by increasing the amount of distractions a person has, although the experiments in this area can be criticised for using impersonal concurrent tasks, which may or may not properly reflect natural processes or individual differences.

Empirical Work (1980s)

In order for thought suppression and its effectiveness to be studied, researchers have had to find methods of recording the processes going on in the mind. One experiment designed with this purpose was performed by Wegner, Schneider, Carter & White. They asked participants to avoid thinking of a specific target (e.g. a white bear) for five minutes, but if they did, they were told then to ring a bell. After this, participants were told that for the next five minutes they were to think about the target. There was evidence that unwanted thoughts occurred more frequently in those who used thought suppression compared to those who were not. Furthermore, there was also evidence that during the second stage, those who had used thought suppression had a higher frequency of target thoughts than did those who had not used thought suppression; later coined the rebound effect. This effect has been replicated and can even be done with implausible targets, such as the thought of a “green rabbit”. From these implications, Wegner eventually developed the “ironic process theory”.

Improved Methodology (1990s)

To better elucidate the findings of thought suppression, several studies have changed the target thought. Roemer and Borkovec found that participants who suppressed anxious or depressing thoughts showed a significant rebound effect. Furthermore, Wenzlaff, Wegner, & Roper demonstrated that anxious or depressed subjects were less likely to suppress negative, unwanted thoughts. Despite Rassin, Merkelbach and Muris reporting that this finding is moderately robust in the literature, some studies were unable to replicate results. However, this may be explained by a consideration of individual differences.

Recent research found that for individuals with low anxiety and high desirability traits (repressors), suppressed anxious autobiographical events initially intruded fewer times than in other groups (low, high, and high defensive anxious groups), but intruded more often after one week. This difference in coping style may account for the disparities within the literature. That said, the problem remains that the cause of the paradoxical effect may be in the thought tapping measures used (e.g. bell ringing). Evidence from Brown (1990) that showed participants were very sensitive to frequency information prompted Clarke, Ball and Pape to obtain participants’ aposterio estimates of the number of intrusive target thoughts and found the same pattern of paradoxical results. However, even though such a method appears to overcome the problem, it and all the other methodologies use self-report as the primary form of data-collection. This may be problematic because of response distortion or inaccuracy in self-reporting.

Behavioural Domain

Thought suppression also has the capability to change human behaviour. Macrae, Bodenhausen, Milne, and Jetten found that when people were asked not to think about the stereotypes of a certain group (e.g. a “skinhead”), their written descriptions about a group member’s typical day contained less stereotypical thoughts. However, when they were told they were going to meet an individual they had just written about, those in the suppression group sat significantly farther away from the “skinhead” (just by virtue of his clothes being present). These results show that even though there may have been an initial enhancement of the stereotype, participants were able to prevent this from being communicated in their writing; this was not true for their behaviour though.

Further experiments have documented similar findings. In one study from 1993, when participants were given cognitively demanding concurrent tasks, the results showed a paradoxical higher frequency of target thoughts than controls. However other controlled studies have not shown such effects. For example, Wenzlaff and Bates found that subjects concentrating on a positive task experienced neither paradoxical effects nor rebound effects – even when challenged with cognitive load. Wenzlaff and Bates also note that the beneficiality of concentration in their study participants was optimised when the subjects employed positive thoughts.

Some studies have shown that when test subjects are under what Wegner refers to as a “cognitive load” (for instance, using multiple external distractions to try to suppress a target thought), the effectiveness of thought suppression appears to be reduced. However, in other studies in which focused distraction is used, long term effectiveness may improve. That is, successful suppression may involve less distractors. For example, in 1987 Wegner, Schneider, Carter & White found that a single, pre-determined distracter (e.g. a red Volkswagen) was sufficient to eliminate the paradoxical effect post-testing. Evidence from Bowers and Woody in 1996 is supportive of the finding that hypnotised individuals produce no paradoxical effects. This rests on the assumption that deliberate “distracter activity” is bypassed in such an activity.

Cognitive Dynamics

When the cognitive load is increased, thought suppression typically becomes less effective. For example, in the white bear experiment, many general distractions in the environment (for instance a lamp, a light bulb, a desk etc.) might later serve as reminders of the object being suppressed (these are also referred to as “free distraction”). Some studies, however, are unable to find this effect for emotional thoughts in hypnotized individuals when one focused distraction is provided. In an attempt to account for these findings, a number of theorists have produced cognitive models of thought suppression. Wegner suggested in 1989 that individuals distract themselves using environmental items. Later, these items become retrieval cues for the thought attempting to be suppressed. This iterative process leaves the individual surrounded by retrieval cues, ultimately causing the rebound effect. Wegner hypothesized that multiple retrieval cues not being forged explains, in part, the effectiveness of focused distraction (i.e. a reduction of mental load). This is because there may be an ideal balance between the two processes; if the cognitive demand that is not too heavy, then the monitoring processes will not supersede it.

Individual differences may also play a role in regards to the ironic thought process.

Thought suppression has been seen as a form of “experiential avoidance”. Experiential avoidance is when an individual attempts to suppress, change, or control unwanted internal experiences (thoughts, feelings, bodily sensations, memories, etc.). This line of thinking supports relational frame theory.

Other Methodologies

Thought suppression has been shown to be a cause of inhibition in several ways. Two commonly-used methods to study this relationship are the list method and the item method. In this list method, participants study two lists of words, one after the other. After studying the first list, some participants are told to forget everything that they have just learned, while others are not given this instruction. After studying both lists, participants are asked to recall the words on both lists. These experiments typically find that participants who were told to forget the first list do not remember as many words from that list, suggesting that they have been suppressed due to the instruction to forget. In the item method, participants study individual words rather than lists. After each word is shown, participants are told to either remember or forget the word. As in experiments using the list method, the words followed by the instruction to forget are more poorly remembered. Some researchers believe that these two methods result in different types of forgetting. According to these researchers, the list method results in inhibition of the forgotten words, but the item method results in some words being remembered better than the others, without a specific relation to forgetting.

Think/No Think Paradigm

A paradigm from 2009 to study how suppression relates to inhibition is the think/no think paradigm. In these experiments, participants study pairs of words. An example of a possible word pair is roach-ordeal. After all the word pairs are learned, the participants see the first word of the pair and are either told to think about the second word (think phase) or not to think about the second word (no think phase). The no think phase is when suppression occurs. Some pairs were never presented after the initial study portion of the study, and these trials serve as the control group. At the end of the experiment, the participants try to remember all of the word pairs based on the first word. Studies could also use the “independent probe” method, which gives the category and first letter of the second word of the pair. Typically, regardless of the method used, results show that the no-think trials result in worse memory than the think trials, which supports the idea that suppression leads to inhibition in memory. Although this methodology was first done using word pairs, experiments have been conducted using pictures and autobiographical memories as stimuli, with the same results.

Research has also shown that doing difficult counting tasks at the same time as a think/no think task leads to less forgetting in the no think condition, which suggests that suppression takes active mental energy to be successful. Furthermore, the most forgetting during the no think phase occurs when there is a medium amount of brain activation while learning the words. The words are never learned if there is too little activation, and the association between the two words is too strong to be suppressed during the no think phase if there is too much activation. However, with medium activation, the word pairs are learned but able to be suppressed during the no think phase.

fMRI studies have shown two distinct patterns of brain activity during suppression tasks. The first is that there is less activity in the hippocampus, the brain area responsible for forming memories. The second is an increase of brain activity in the dorsolateral prefrontal cortex, especially in cases where suppression is harder. Researchers think that this region works to prevent memory formation by preventing the hippocampus from working.

This methodology can also be used to study thought substitution by adding an instruction during the no think phase for participants to think of a different word rather than the word being suppressed. This research shows that thought substitution can lead to increased levels of forgetting compared to suppression without a thought substitution instruction. This research also suggests that thought substitution, while used as a suppression strategy during the no think phase, may work differently than suppression. Some researchers argue that thinking of something different during the no think phase forms a new association with the first word than the original word pair, which results in interference when using this strategy, which is different than the inhibition that results from simply not thinking about something.

Dream Influence

Dreams occur mainly during the rapid eye movement (REM) sleep and are composed of images, ideas, emotions, and sensations. Although more research needs to be done on this subject, dreams are said to be linked to the unconscious mind. Thought suppression has an influence on the subject matter of the unconscious mind and by trying to restrain particular thoughts, there is a high chance of them showing up in one’s dreams.

Ironic Control Theory

Ironic control theory, also known as “ironic process theory”, states that thought suppression “leads to an increased occurrence of the suppressed content in waking states”. The irony lies in the fact that although people try not to think about a particular subject, there is a high probability that it will appear in one’s dreams regardless. There is a difference for individuals who have a higher tendency of suppression; they are more prone to psychopathological responses such as “intrusive thoughts, including depression, anxiety and obsessional thinking”. Due to these individuals having higher instances of thought suppression, they experience dream rebound more often.

Cognitive load also plays a role in ironic control theory. Studies have shown that a greater cognitive load results in an increased possibility of dream rebound occurring. In other words, when one tries to retain a heavy load of information before going to sleep, there is a high chance of that information manifesting itself within the dream. There is a greater degree of dream rebound in those with a higher cognitive load opposed to those whose load was absent. With the enhancement of a high cognitive load, ironic control theory states thought suppression is more likely to occur and lead to dream rebound.

Dream Rebound

Dream rebound is when suppressed thoughts manifest themselves in one’s dreams. Self-control is a form of thought suppression and when one dreams, that suppressed item has a higher chance of appearing in the dream. For example, when an individual is attempting to quit smoking, they may dream about themselves smoking a cigarette. Emotion suppression has also been found to trigger dream rebound. Recurrence of emotional experiences act as pre-sleep suggestions, ultimately leading to the suppressed thoughts presenting themselves within the dream. One effecting factor of dream rebound is the changes in the prefrontal lobes during rapid-eye movement sleep. Suppressed thoughts are more accessible during REM sleep, as a result of operating processes having a diminished effectiveness. This leads to pre-sleep thoughts becoming more available “with an increased activity of searching for these suppressed thought[s]”. There are other hypotheses regarding REM sleep and dream rebound. For instance, weak semantic associations, post REM sleep, are more accessible than any other time due to weak ironic monitoring processes becoming stronger. More research is needed to further understand what exactly causes dream rebound.

What is Inhibitory Control?


Inhibitory control, also known as response inhibition, is a cognitive process – and more specifically an executive function – that permits an individual to inhibit their impulses and natural, habitual, or dominant behavioural responses to stimuli (e.g. prepotent responses) in order to select a more appropriate behaviour that is consistent with completing their goals.

Self-control is an important aspect of inhibitory control. For example, successfully suppressing the natural behavioural response to eat cake when one is craving it while dieting requires the use of inhibitory control.

The prefrontal cortex, caudate nucleus, and subthalamic nucleus are known to regulate inhibitory control cognition. Inhibitory control is impaired in both addiction and attention deficit hyperactivity disorder. In healthy adults and ADHD individuals, inhibitory control improves over the short term with low (therapeutic) doses of methylphenidate or amphetamine. Inhibitory control may also be improved over the long-term via consistent aerobic exercise.


An inhibitory control test is a neuropsychological test that measures an individual’s ability to override their natural, habitual, or dominant behavioural response to a stimulus in order to implement more adaptive goal-oriented behaviours. Some of the neuropsychological tests that measure inhibitory control include the Stroop task, go/no-go task, Simon task, Flanker task, anti-saccade tasks, delay of gratification tasks, and stop-signal tasks.

Gender Differences

Females tend to have a greater basal capacity to exert inhibitory control over undesired or habitual behaviours and respond differently to modulatory environmental contextual factors relative to males. For example, listening to music tends to significantly improve the rate of response inhibition in females, but reduces the rate of response inhibition in males.

Linking Brain Imagery, Brain Tumours, and Cognitive & Mental Disorders in Adults

Research Paper Title

Brain tumours, cognitive and mental disorders in adults.


Cognitive and mental disorders are observed in 15-20% of brain tumours, and can be the first symptoms.

The severity of cognitive deficits varies from attention and reasoning disorders to major syndromes such as delirium, amnesic syndrome or dementia.

Mental disorders range from apathy, irritability to major depressive or psychotic symptoms.

Cognitive and mental disorders are related to many factors including the localisation and nature of the tumour, peritumoral and remote changes, and personal susceptibility.

The diagnosis of brain tumour is presently made by brain imagery, but the difficulty remains to determine when imagery is to be used in cognitive or mental disorders.


Derouesne, C. (2020) Brain tumors, cognitive and mental disorders in adults. Geriatrie et Psychologie Neuropsychiatrie du Vieillissement. 13(2), pp.187-194. doi: 10.1684/pnv.2015.0533.

Is There an Association between Cardiovasular Disease & Executive Function in Those with Bipolar Disorder?

Research Paper Title

Cumulative Cardiovascular Disease Risk and Triglycerides Differentially Relate to Subdomains of Executive Function in Bipolar Disorder; preliminary findings.


Cardiovascular disease is disproportionally prevalent in bipolar disorder (BD) and has been linked to cognition in preliminary studies. The researchers evaluate the association between known risk factors for cardiovascular disease and executive function in BD patients compared to healthy controls.


In a sample of n=57 individuals (n=23 BD, n=34 controls) they assessed two subdomains of executive function; cognitive flexibility (using the Trail Making Test – Part B) and cognitive inhibition (using the Stroop Colour Word Interference Task). Cardiovascular risk was assessed by means of serum triglyceride levels, body mass index (BMI) and waist circumference, as well as dietary saturated fat intake and a sex-specific cumulative cardiovascular risk score calculated using the Framingham Heart Study method.


Patients with BD had higher BMI and waist circumference, with more BD patients categorised as having central obesity than controls. In the BD group only, higher triglyceride levels were associated with worse cognitive flexibility, and elevated cumulative cardiovascular disease risk was associated with worse cognitive inhibition. No correlations between cardiovascular risk factors and executive function were evident in the control group.

The study was limited by the small sample size and should be considered hypothesis-generating.


The associations between triglyceride levels, cumulative cardiovascular disease risk and executive functioning evident in BD in this study preliminarily indicate the potential for mechanistic overlap of physical health and cognitive function in the disorder.


Van Rheenen, T.E., McIntyre, R.S., Balanza-Martinez, V., Berk, M. & Rossell, S.L. (2020) Cumulative Cardiovascular Disease Risk and Triglycerides Differentially Relate to Subdomains of Executive Function in Bipolar Disorder; preliminary findings. Journal of Affective Disorders. 278, pp.556-562. doi: 10.1016/j.jad.2020.09.104. Online ahead of print.

What is the Association with Several Physical, Mental, & Cognitive Health Outcomes with Gait Speed in Older Adults?

Research Paper Title

Clinical and Ambulatory Gait Speed in Older Adults: Associations With Several Physical, Mental, and Cognitive Health Outcomes.


Although clinical gait speed may indicate health and wellbeing in older adults, there is a lack of studies comparing clinical tests with ambulatory gait speed with regard to several health outcomes.

The objective of this study was to examine the associations of clinical gait speed, measured by the 2.44 meter walk test and the ambulatory gait speed with several physical, mental, and cognitive health outcomes in older adults.

A cross-sectional design was used.


The study population comprised 432 high-functioning community-dwelling older adults (287 women) aged between 65 and 92.

Clinical and ambulatory gait speeds were measured using the 2.44 m walk test and a portable gait analysis device, respectively.

Multiple linear regressions were used to examine the association of clinical and ambulatory gait speeds with several health outcomes (BMI, waist circumference, systolic and diastolic blood pressure, chronic conditions, self-rated health, exhaustion, upper and lower body strength, physical and mental health status, cognitive status and self-rated cognitive status).


The results showed that the average gait speed for clinical and ambulatory measures cannot be directly compared.

Clinical gait speed was associated with 7 health outcomes, while the ambulatory gait speed was associated with 6 health outcomes.

The significant associations between measures of gait speed and the health outcomes converged in 5 of the 13 health outcomes studied, however, the strength of associations were singly different between measures.

The short monitoring time, the inability to distinguish between the ambulatory gait speed inside the home and outdoor gait speed, and the under-representative sample are limitations of the study.


The results indicated differences in the number and strength of associations between clinical and ambulatory gait speed.

Both measures have construct validity because they have been associated with physical and health outcomes, however, they may have different predictive validity.

Further research should be done to compare their predictive validity in longitudinal designs.


De la Cámara, M.Á., Higueras-Fresnillo, S., Sadarangani, K.P., Esteban-Cornejo, I., Martinez-Gomez, D. & Veiga, Ó.L. (2020) Clinical and Ambulatory Gait Speed in Older Adults: Associations With Several Physical, Mental, and Cognitive Health Outcomes. Physical Therapy. pii: pzz186. doi: 10.1093/ptj/pzz186. [Epub ahead of print].

Cognitive Subgroups of Schizophrenia: Are There Brain Morphological & Functional Features?

Research Paper Title

Brain morphological and functional features in cognitive subgroups of schizophrenia.


Previous studies have reported different brain morphologies in different cognitive subgroups of patients with schizophrenia. The researchers aimed to examine the brain structures and functional connectivity in these cognitive subgroups of schizophrenia.


The researchers compared brain structures among healthy controls and cognitively deteriorated and preserved subgroups of patients with schizophrenia according to the decline in intelligence quotient.

Connectivity analyses between subcortical regions and other brain areas were performed using resting-state functional magnetic resonance imaging among the groups.


Whole brain and total cortical gray matter, right fusiform gyrus, left pars orbitalis gyrus, right pars triangularis, left superior temporal gyrus and left insula volumes and bilateral cortical thickness were decreased in the deteriorated group compared to the control and preserved groups.

Both schizophrenia subgroups had increased left lateral ventricle, right putamen and left pallidum and decreased bilateral hippocampus, left precentral gyrus, right rostral middle frontal gyrus and bilateral superior frontal gyrus volumes compared with controls.

Hyperconnectivity between the thalamus and a broad range of brain regions was observed in the deteriorated group compared to connectivity in the control group, and this hyperconnectivity was less evident in the preserved group.

The researchers also found hyperconnectivity between the accumbens and the superior and middle frontal gyri in the preserved group compared with connectivity in the deteriorated group.


These findings provide evidence of prominent structural and functional brain abnormalities in deteriorated patients with schizophrenia, suggesting that cognitive subgroups in schizophrenia might be useful biotypes to elucidate brain pathophysiology for new diagnostic and treatment strategies.


Yasuda, Y., Okada, N., Nemoto, K., Fukunaga, M., Yamamori, H., Ohi, K., Koshiyama, D., Kudo, N., Shiino, T., Morita, S., Morita, K., Azechi, H., Fujimoto, M., Miura, K., Watanabe, Y., Kasai, K. & Hashimoto, R. (2019) Brain morphological and functional features in cognitive subgroups of schizophrenia. Psychiatry and Clinical Neurosciences. doi: 10.1111/pcn.12963. [Epub ahead of print].